Increased RNA editing in maternal immune activation model of neurodevelopmental disease.
Hadas Tsivion-VisbordEli KopelAriel FeiglinTamar SoferRan BarzilayTali Ben-ZurOrly YaronDaniel OffenErez Y LevanonPublished in: Nature communications (2020)
The etiology of major neurodevelopmental disorders such as schizophrenia and autism is unclear, with evidence supporting a combination of genetic factors and environmental insults, including viral infection during pregnancy. Here we utilized a mouse model of maternal immune activation (MIA) with the viral mimic PolyI:C infection during early gestation. We investigated the transcriptional changes in the brains of mouse fetuses following MIA during the prenatal period, and evaluated the behavioral and biochemical changes in the adult brain. The results reveal an increase in RNA editing levels and dysregulation in brain development-related gene pathways in the fetal brains of MIA mice. These MIA-induced brain editing changes are not observed in adulthood, although MIA-induced behavioral deficits are observed. Taken together, our findings suggest that MIA induces transient dysregulation of RNA editing at a critical time in brain development.
Keyphrases
- crispr cas
- resting state
- white matter
- cerebral ischemia
- mouse model
- genome wide
- functional connectivity
- high glucose
- diabetic rats
- drug induced
- pregnant women
- traumatic brain injury
- sars cov
- gene expression
- copy number
- bipolar disorder
- transcription factor
- physical activity
- type diabetes
- nucleic acid
- mass spectrometry
- single cell
- endothelial cells
- high resolution
- subarachnoid hemorrhage
- stress induced
- weight gain
- childhood cancer